Courtesy of Global Health Media Project
Neonatal jaundice, is one of the commonest issues affecting newborns. It is observed in upto 60% of term infants and 80% of preterm infants. Clinically, jaundice appears as yellowness of skin due to of elevated bilirubin ( a breakdown product of hemoglobin) levels above 85-120 umol/L, or 5-6 mg/dL.
Most jaundice is "physiologic" and self-limited. Physiologic jaundice normally occurs postpartum day 2-3, peaking by the fourth day, and resolving by 7 days. Premature infants have longer duration.
However, diffentiation between physiologic jaundice, which does not require any intervention and pathologic jaundice, which if untreated is potentially neurotoxic and most often lethal is of utmost clinical importance.
Daniel is an infant born to a mother who received no prenatal care during her pregnancy. Based on her estimation, Daniel was born at 39 weeks gestational age. Her labour and delivery were uneventful, and he was born with APGAR scores of 9 and 9 at 1 and 5 minutes, respectively. However, his nurse immediately noticed that he had a strong yellow colour to his skin, and because concerned about the possibility of jaundice.
jaundice, from Wikipedia
Most of the cases of neonatal jaundice is physiological in nature and is not worrisome. It has some specific features:
In preterm babies, the peak may be seen a little later and biliribun levels may be slightly higher and lasts slightly longer.
The fact that the nature of jaundice (i.e whether physiological of pathological) cannot be determined by a single examination; it has to be observed over a period of time, and if required investigations done and only then commented upon.
Mothers are often anxious on hearing the word “jaundice” It is important to counsel them that physiological jaundice is benign and has bo long term sequlae either. In developing nations of South Asia, mothers often want to give babies extra glucose water. This should be counselled against and breast feeding may be advised instead.
Various causes of jaundice are described below. Alongside these, increased circulating bilirubin is seen with:
Newborns have high levels of hemoglobin, which is converted to biliverdin and then bilirubin. Uncongugated bilirubin is not water-soluble, and is transported through the blood on albumin to the liver, where it is congugated by gluconuryl transferase to form 'direct' bilirubin, water-soluble bilirubin that can be excreted into the urine or stool.
Physiologic jaundice occurs due to increased hematocrit, slow functioning of glucuronyl transferase, and increased enterohepatic circulation.
Increased destruction of bilirubin, such as by hemolysis, hematoma, or other causes, will result in high levels of uncongugated bilirubin.
Decreased gastrointestinal motility will also increase bilirubin levels.
Direct hyperbilirubinemia can be increased by infection, metabolism disorders, liver dysfunction, or obstruction of the bile ducts.
Bilirubin retention is increased by prematurity, acidosis, hypoalbuminemia, and dehydration.
obstruction (eg biliary atresia)
Early (< 24 hours)
Early presentation is almost always pathological. Common causes include:
Typical (24-96 hours)
Jaundice may be present at birth or may reappear later at time. Though mothers are usually alert and will inform the health care provider, a routine check for jaundice is recommended for each visit in the entire neonatal period.
age of infant (as described above)
pregnancy and birth history
general state of infant
feeding type and history
A very important feature of neonatal jaundice (whether pathological or physiological) is the fact that its locational extent can be used to estimate bilirubin levels:
Routine bloodwork will reveal relative levels of direct and indirect bilirubin.
Investigations are required if jaundice appears pathological clinicially (is seen within the first day, if jaundice persists beyond one week). Identification of the cause is usually straightforward.
Bilirubin is most frequently measured by transcutaneous means.
Bloodwork is required to detect levels of direct (conjugated) bilirubin. This can be subtracted from total levels to yield indirect, or uncongugated bilirubin.
If causes are unclear, tests to consider include:
Other tests to consider include:
If bilirubin is conjugated, consider:
A chest X ray may be done to assess for pneumonia, if infection is a concern.
If direct bilirubin levels are elevated, consider:
Infants with physiological jaundice require only monitoring. If breastfeeding is a concern, discuss strategies for effective feeds. This can include latching, adequate hydration in the mother, and pumping as necessary. Supplementation may be necessary as the milk supply comes in.
If pathologic jaundice is suspected, all efforts should be pursued to prevent the development of long-term damage (described below). Early feeding and maintenance of adequate hydration is essential. Acidosis/hypoxia/hypothermia/hypoglycaemia is to be prevented. Also appropriate antibiotics should be given in cases of infection, and many physicians advocate the use of prophylactic antibiotics. Administration of Vitamin K injections are also predispose to the development of kernicterus by aggravating haemolysis.
The most common treatment is phototherapy, which alters bilirubin in blood vessels with ultraviolet light to allow for excretion in the urine.
Treatments, in increased order of efficacy, include:
Phototherapy is often given when bilirubin levels reach 10 to 12 mg/dl for preterms and 15mg/dl for term infants. Specific guidelines for directing treatment can be found according to AAP phototherapy nomogram.
Complications of treatment include parental distress (especially about eye-covering), interference with bonding and feeding, watery stools, increased temperature, skin rashes, and bronzed-baby syndrome (if high levels of direct bilirubin are present).
If phototherapy is insufficient, double-volume exchange transfusion done through the umbilical vein can be effective, though with serious complications. The decision for exchange transfusion is guided by a multitude of factors in addition to the levels of unconjugated bilirubin levels like gestational maturity , postnatal age, presence or absence of perinatal distress factors and cause of jaundice.Other newer treatments include tin mesoporphyrin.
Direct hyperbilirubinemia requires treatment of the underlying condition.
Elevated levels of unconjugated bilirubin can cross the blood-brain barrier and enter the brain, where it acts as a neurotoxin and causes CNS damage, termed kernicterus, or bilirubin encephalopathy. Kernicterus can cause:
Conjugated (direct) bilirubin cannot enter the brain and so does not cause kernicterus. However, the conditions that lead to jaundice can have life-threatening consequences of their own.